Cytokine Phenotypes After the Host's Response During Chronic Lung Inflammation
慢性肺部炎症期间宿主反应后的细胞因子表型
基本信息
- 批准号:8197282
- 负责人:
- 金额:$ 37.49万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2008
- 资助国家:美国
- 起止时间:2008-12-01 至 2013-11-30
- 项目状态:已结题
- 来源:
- 关键词:AnimalsAutoimmune DiseasesAutomobile DrivingCell physiologyCellsChronicChronic DiseaseChronic lung diseaseClinicalClinical ManagementCollagenCommunicable DiseasesConnective Tissue DiseasesDendritic CellsDeteriorationDiseaseDisease ProgressionEnvironmentEtiologyEvolutionExperimental ModelsFibroblastsFibrosisGrowthHamman-Rich syndromeImmuneImmune Cell ActivationImmune responseInfectionInjuryInterleukin-13Interleukin-4Interstitial Lung DiseasesInvestigationLabelLaboratoriesLeadLesionLungLung InflammationLung diseasesMaintenanceModelingMusOutcomePathologyPhenotypePredispositionProteinsResearchRespiratory physiologyRiskStructure of parenchyma of lungTestingTissuesTransforming Growth Factor betaViralVirus Diseasescytokinedesigngammaherpesvirusinterstitialpathogenresearch studyresponse
项目摘要
Chronic interstitial lung disease is observed in a variety of disorders, including infectious diseases,
autoimmune disorders of connective tissue, and disorders where the etiology is unknown, such as idiopathic
pulmonary fibrosis. While the etiology and mechanism of progression of many of these lung disorders are not
known, the exacerbated progression of the disease may be dictated by the host responding to a subsequent
pathogen superimposed on the initial etiologic agent. This "second hit" triggers a dynamic interaction in the
lung between the inciting agent, immune cells, and structural cells of the lung, culminating in fibroblast
activation, proliferation and fibrosis. Understanding the mechanisms responsible for the exacerbation and
progression of lung disease chronicity and fibrosis are the broad, long-term objectives of this application. We
hypothesize that the host's response to a persistent etiologic agent may predispose lung tissue to an
environment of reparative and immunoregulatory cytokines, placing the lungs at risk for a viral infection, which
mechanistically contributes to disease chronicity by maintaining a unique cytokine phenotype, altering
dendritic cell function, and driving fibroblast activation. We have designed experiments to test this hypothesis
and determine if the progression and maintenance of chronic lung inflammation are infuenced by the cytokine
phenotype and the host's response to a subsequent viral pathogen superimposed on the initial etiologic agent,
constituting a "two hit" mechanism for disease progression. We will focus on mechanisms which lead to a
minimally fibrotic lung lesion, induced by type 1 cytokines, versus a fibrotic response, induced by type 2
cytokines, and determine their impact on a subsequent challenging with murine gammaherpesvirus (MHV68).
Our specific Aims include: 1) To assess the mechanism(s) whereby MHV68 infection alone or superimposed
on a polarized cytokine phenotype alters the host response and subsequent lung pathology in experimental
models of chronic lung inflammation; 2) To determine the mechanistic contribution of an MHV68-derived gene
product on the evolving chronic lung pathology associated with a type 1 or type 2 cytokine tissue phenotype;
and 3) To assess the mechanistic contribution of dendritic cell subsets during MHV68 infection to the chronicity
and fibrosis of the lung response in animals with developing type 1 or type 2 cytokine phenotypes.
慢性间质性肺病见于多种疾病,包括感染性疾病,
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Steven Lynn Kunkel其他文献
Steven Lynn Kunkel的其他文献
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{{ truncateString('Steven Lynn Kunkel', 18)}}的其他基金
The Immune Response to Pathogens is Controlled by the Cytokine-Induced Epigenetics Signature
对病原体的免疫反应由细胞因子诱导的表观遗传学特征控制
- 批准号:
9526608 - 财政年份:2017
- 资助金额:
$ 37.49万 - 项目类别:
Cytokine Phenotypes After the Host's Response During Chronic Lung Inflammation
慢性肺部炎症期间宿主反应后的细胞因子表型
- 批准号:
7578408 - 财政年份:2008
- 资助金额:
$ 37.49万 - 项目类别:
Cytokine Phenotypes After the Host's Response During Chronic Lung Inflammation
慢性肺部炎症期间宿主反应后的细胞因子表型
- 批准号:
8387726 - 财政年份:2008
- 资助金额:
$ 37.49万 - 项目类别:
A multi-scale and multi-system approach to understand granuloma formation in TB
了解结核病肉芽肿形成的多尺度、多系统方法
- 批准号:
7498649 - 财政年份:2008
- 资助金额:
$ 37.49万 - 项目类别:
Cytokine Phenotypes After the Host's Response During Chronic Lung Inflammation
慢性肺部炎症期间宿主反应后的细胞因子表型
- 批准号:
7993581 - 财政年份:2008
- 资助金额:
$ 37.49万 - 项目类别:
A multi-scale and multi-system approach to understand granuloma formation in TB
了解结核病肉芽肿形成的多尺度、多系统方法
- 批准号:
7877856 - 财政年份:2008
- 资助金额:
$ 37.49万 - 项目类别:
Cytokine Phenotypes After the Host's Response During Chronic Lung Inflammation
慢性肺部炎症期间宿主反应后的细胞因子表型
- 批准号:
7743005 - 财政年份:2008
- 资助金额:
$ 37.49万 - 项目类别:
A multi-scale and multi-system approach to understand granuloma formation in TB
了解结核病肉芽肿形成的多尺度、多系统方法
- 批准号:
7659589 - 财政年份:2008
- 资助金额:
$ 37.49万 - 项目类别:
Dynamic Effects of Chemokines on Systematic inflammation
趋化因子对系统炎症的动态影响
- 批准号:
7108652 - 财政年份:2005
- 资助金额:
$ 37.49万 - 项目类别:
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